J Cardiol 2007 May; 49（5）: 267– 271

Rare Survival in a Patient With
Severe Complications of Acute
Myocardial Infarction : A Case
ReportNoriaki

TAKAMA, MD

Hiroshi

HOSHIZAKI, MD＊＊Shigeto NAITO, MD＊Shigeru OSHIMA, MD, FJCC
Koichi＊TANIGUCHI, MD, FJCC

Masahiko KURABAYASHI, MD, FJCC
Abstract ─────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────
A 50-year-old man presented with acute myocardial infarction. Coronary angiography showed the left
anterior descending artery（segment 6）was totally occluded. Direct percutaneous transluminal coronary
angioplasty was performed, but a distal embolism occurred by the procedure. Consequently, he sufferedcardiogenic shock and sustained ventricular tachycardia/fibrillation which exacerbated his condition.
Finally, the patient was successfully treated with catheter ablation and cryosurgery to control the incessantventricular arrhythmias, and partial left ventricular volume reduction and coronary artery bypass grafting
to improve contractile performance. His left ventricular contractility did not improve, but the incessantventricular arrhythmias could be controlled. His condition remarkably improved and he was discharged on
foot. This patient with severe complications of acute myocardial infarction showed unusually goodresponse and recovery.
────────────────────────────────────────────────────────────────────────────────────────────────────────────────────J Cardiol 2007 May; 49（5）: 267 −271

Key Words■ Myocardial infarction, treatment（acute）■ Shock（cardiogenic）■ Arrhythmias（fatal, cryosurgery）■ Ventricular function（left ventricular volume reduction）

INTRODUCTION
Generally, both intraaortic balloon pumping（IABP）and percutaneous cardiopulmonary support（PCPS）
are effective for myocardial infarction withcardiogenic shock.1−4）However, these treatments
are not effective in patients with severe complications causing exacerbation of acute myocardialinfarction. We describe a remarkable patient who
survived after treatment by cryosurgery, left ventricular volume reduction, and coronary artery

bypass grafting（CABG）.
CASE REPORT
A 50-year-old man had a 28-year history ofuntreated hypertension. The patient developed anterior chest pain and electrocardiography showed ST
elevations in leads Ⅰ, aⅤL , Ⅴ2 −Ⅴ6. Two hours
later, he was transferred to our hospital with continuing chest pain. Chest radiography revealed
enlargement of the cardiac silhouette and pulmonary edema（Fig. 1）. The ST segments remained──────────────────────────────────────────────
群馬大学大学院医学系研究科 臓器病態内科学 : 〒 371−8511 群馬県前橋市昭和町 3−39−22 ; ＊群馬県立心臓血管センター
循環器内科，群馬Medicine & Biological Science, Gunma University Graduate School of Medicine, Maebashi, Gunma ; ＊ Cardiology Division, Gunma
Prefectural Cardiovascular Center, Gunma
Address for correspondence : TAKAMA N, MD, Medicine & Biological Science, Gunma University Graduate School of Medicine,Showa-machi 3−39−11, Maebashi, Gunma 371−8511 ; E-mail : goritakama@db3.so-net.ne.jp
Manuscript received January 19, 2007 ; revised February 9, 2007 ; accepted February 9, 2007267

268Takama, Hoshizaki, Naito et alIIIV1V2IIIV3aVR
V4aVLV5aVFV6

Fig. 1 Chest radiograph showing cardiomegaly（cardiothoracic ratio of 67%）and significant congestion
in both lungs

elevated in leads Ⅰ, aⅤL , Ⅴ2 −Ⅴ6（Fig. 2）.
Transthoracic echocardiography revealed akinesis
at anteroseptal wall area and diffuse hypokinesis
with left ventricular end-diastolic dimension（LVDd）
of 87 mm, and left ventricular end-systolic dimension（LVDs）of 80 mm. The ejection fraction was33%. Laboratory examinations showed elevation inthe serum creatine kinase（CK）activity（CK : 617
IU/l, CK-MB : 62 IU/l）. Based on the results ofthese examinations, acute myocardial infarction
was suspected.
Emergent coronary angiography showed the left
anterior descending artery（LAD ; segment 6）was
totally occluded without collateral circulation. The
right coronary artery and left circumflex coronary
artery were normal. During percutaneous transluminal coronary angioplasty（PTCA）, a guide wire
was easily passed through the culprit lesion and aPTCA balloon（3.0 mm）was inflated. However, adistal embolism was produced by the procedure.
The LAD（segment 7）, first diagonal branch（D1）and septal branch were almost totally occluded.
Unfortunately, aspiration therapy was impossible toperform at that time. IABP was placed to treat cardiogenic shock and to increase coronary flow. The
patient was treated with aspirin（81 mg/day）, ticlopidine（200 mg/day）, and heparin sodium（10,0001,000 msec

Fig. 2 Electrocardiogram showing ST segment elevation in leads Ⅰ, aⅤL, Ⅴ2−Ⅴ6 with sinus tachycardia（102 beats/min）

U/day）. The maximum CK release was 4,196 IU/l.
The patient developed sustained ventriculartachycardia（VT）resulting in near-syncope on theday after PTCA（Fig. 3）. Anti-arrhythmic agents（lidocaine : 120 mg/hr, amiodarone : 800 mg/day）were administered to treat, and the defibrillator wasused, but were not effective and his vital signs wereexacerbated. A PCPS was initiated with IABP
（PCPS at 4 l/min）. The blood pressure was maintained at 80 mmHg, with a cardiac output of 1.9l/min and a mean pulmonary capillary wedge pressure of 19 mmHg. However, the sustained VT persisted and the patient developed sustained ventricular fibrillation（VF）. The VT and VF continued for
2 days. The sustained VF resulted in low cardiac
output and multiple organ failure. Blood examination found hemoglobin 10.3 g/dl, platelet count was
6.0 × 104/μl, blood urea nitrogen was 65 mg/dl,
and serum creatinine concentration was 2.5 mg/dl.
Four days after admission, an electrophysiological study to determine the focus of the VT showed
the earliest electrical potential originated from theregion from the septum to the middle inferior wall,
and almost perfect mapping was shown（Fig. 4）.
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Severe Complications of Acute Myocardial Infarction

ⅠaVR

V1V4ⅡaVLV2V5ⅢaVF

V3V6Fig. 3 Electrocardiogram showing sustained ventricular tachycardia with complete right bundle
branch block and left axis deviation pattern
Cycle length is 280 msec.

Pacing（ap ex） Clinical VT

Pacing（ap ex） Clinical VTⅠV1ⅡV2Ⅲ

V3aVV4aVV5aVV6Fig. 4 Left ventricular pace mapping showing almostperfect mapping
In this position, entrainment phenomenon is observed（not shown）.
VT ＝ ventricular tachycardia.

Then catheter ablation was performed.
Unfortunately, it was impossible to completelyinhibit the incessant potentially fatal arrhythmias.
Finally, the following strategy was decided. We
decided to perform cryosurgery to treat the incessant arrhythmias, then to perform left ventricularvolume reduction for wall motion improvement,
and finally to perform CABG. Accordingly, left
ventricular mapping was performed again, andcryosurgery was performed to treat the sustained
VT for 180 sec from the left ventricular septum toJ Cardiol 2007 May; 49（5）: 267– 271

269Fig. 5 Postoperative clinical course
After cryosurgery, partial left ventricular volume reduction, and coronary artery bypass grafting operation,
PCPS could be stopped on the fourth postoperative day.
Inotropic agents could be discontinued on the 40th postoperative day.
SBP ＝ systolic blood pressure ; PCPS ＝ percutaneous
cardiopulmonary support ; IABP ＝ intraaortic balloon
pumping ; DOA ＝ dopamine ; DOB ＝ dobutamine ;CHDF ＝ continuous hemodiafiltration ; POD ＝ postoperative day.

the inferior wall. Moreover, antiarrhythmic agents（a m i o d a r o n e : 5 0 m g / d a y a n d d , l - s o t a l o l :80 mg/day）were also administered. The cryosurgery
focus of the sustained VT was marked in catheter
ablation, and was used as a medical guideline. The
sustained VT and VF were completely ameliorated.
Partial left ventricular volume reduction surgery
was successfully performed. We appropriately
excised the myocardium detected to be the infarct
area. However, the border of the acutely infarcted
myocardium was impossible to differentiate accurately, because it also contained an area of very
recent infarction. Postoperative measurement oftransthoracic echocardiography revealed LVDd of70 mm, LVDs of 59 mm, and ejection fraction of33%, and left ventricular contraction was impossible to improve. The patient suffered from hypertension, but there was no evidence to show hypertensive heart disease. Endomyocadial biopsy foundonly accumulation of neutrophile and fibrosis.
CABG was also performed using a saphenous vein
grafted to the LAD.
The postoperative clinical course for this patientis summarized in Fig. 5. Seven months after admission, repeat coronary angiography was performed.
The LAD（segment 7）, D1 and septal branch weretotally occluded, as before. However, the bypass
graft was patent. Left ventriculography revealed

270

Takama, Hoshizaki, Naito et al

severe diffuse hypokinesis with apical aneurysm.
The ejection fraction was 22%. Electrophysiological study was also performed, but no potentially fatal arrhythmias could be induced by frequent right ventricular stimulation.
DISCUSSION
This patient presented with severe acute myocardial infarction. He suffered cardiogenic shock andincessant potentially fatal arrhythmias after treating
the acute myocardial infarction. Generally, both
IABP and PCPS are effective treatments formyocardial infarction with cardiogenic shock.1−4）
However, they were not effective for this patientand his physical condition was exacerbated,because the incessant arrhythmias and cardiogenic
shock were sustained. Our initial treatment wasPTCA, which is a standard treatment for acute
myocardial infarction. However, PTCA was unsuccessful due to distal embolism, and was the main
reason for this patient to fall into this miserable
state.
As a result, we were obliged to follow a double
strategy. Firstly, cryosurgery was performed totreating the incessant arrhythmias and both partial
left ventricular volume reduction and CABG were
performed to treat the cardiogenic shock. The mosteffective treatment was cryosurgery, which controlled the incessant arrhythmias immediately.
Arrhythmias after acute myocardial infarction havebeen treated by catheter ablation in the treatment of
VT in selected patients with healed myocardial
infarction.5−9）Catheter ablation can now be used tofatal arrhythmias caused by non-healed myocardial
要infarction, but few case reports have described fatalarrhythmias with non-healed myocardial infarction.10,11）In our patient, mapping of the VT focus
showed that cryosurgery would be effective.
Given that partial left ventricular volume reduction was performed in the subacute phase of
myocardial infarction, the extensive dyskinetic areaof the myocardium was impossible to reduce completely. In the chronic phase, left ventricular contractility did not improve despite partial left ventricular volume reduction and patent coronary
bypass graft. This showed the border of the acutely
infarcted myocardium was impossible to differentiate accurately. Whether partial left ventricular volume reduction was effective is doubtful. On theother hand, our patient came out of cardiogenic
shock, and survived without PCPS and IABP. We
could not use aspiration therapy and nifekalant,
which are common treatments for such a patient.
However, we believed that our treatment was thebest at that time and his survival depended on all
medical treatments.
This case indicates that the first principle is to beable to control incessant fatal arrhythmias, the second principle is to improve cardiogenic shock using
partial left ventricular volume reduction andCABG. Our patient had suffered from incessantarrhythmias and multiple organ failure for several
days, but survived and was discharged on foot. Thisis a remarkable survival in a patient with severe
complications of acute myocardial infarction treated by cryosurgery, left ventricular volume reduction, and CABG.
約

重度合併症を発症した急性心筋梗塞患者救命の 1 例
高間典明

星 崎洋内藤滋人

大 島茂

谷口興一

倉林正彦

症例は急性心筋梗塞に罹患した 50 歳，男性．心臓カテーテル検査では左前下行枝（分節 6）が完全閉塞であった．経皮的冠動脈形成術を施行したものの，最終的には遠位部に血栓性閉塞をきた
した．その結果，心原性ショックと持続性心室頻拍ならびに心室細動が出現し状態悪化の原因となった．最終的には不整脈をコントロールする目的で，カテーテルアブレーションならびに冷凍外科療法を施行し，心機能改善する目的で左室縮小術と冠動脈バイパス術を施行した．心機能の改善は認められなかったが，持続性の心室性不整脈はコントロールすることができた．臨床経過は著明に改善し，最終的には独歩で退院することができた．急性心筋梗塞に伴う重度合併症を持つ症例を救命することができたので報告した．

J Cardiol 2007 May; 49（5）: 267−271
J Cardiol 2007 May; 49（5）: 267– 271

Severe Complications of Acute Myocardial Infarction

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